Protein misfolding and mitochondrial dysfunction in glaucoma DOI Creative Commons
Arunkumar Venkatesan, Audrey M. Bernstein

Frontiers in Cell and Developmental Biology, Journal Year: 2025, Volume and Issue: 13

Published: April 25, 2025

Glaucoma is a leading cause of irreversible blindness worldwide. Elevated intraocular pressure caused by restricted outflow the aqueous humor leads to degeneration retinal ganglion cells (RGCs) and their axons. Emerging evidence suggests that pathological mechanisms relating protein folding mitochondrial dysfunction are significant factors in disease onset different types open-angle glaucoma. In this review, we discuss these defects three distinct glaucoma: primary glaucoma (POAG), normal tension (NTG), exfoliation (XFG). Genetic mutations linked previously mentioned glaucoma, including those myocilin (MYOC), optineurin (OPTN), lysyl oxidase 1 (LOXL1), disrupt homeostasis, endoplasmic reticulum stress, activation unfolded response impaired autophagic degradation. These contribute trabecular meshwork cell apoptosis. addition defects, also associated with progression damage death RGCs. Factors such as oxidative an altered fission-fusion balance, mitophagy dysregulation make RGCs vulnerable optic nerve degeneration. The crosstalk between underscores complexity pathogenesis offers potential targets for therapeutic intervention. Strategies aimed at restoring enhancing function, mitigating cellular stress responses hold promise neuroprotection

Language: Английский

Protein misfolding and mitochondrial dysfunction in glaucoma DOI Creative Commons
Arunkumar Venkatesan, Audrey M. Bernstein

Frontiers in Cell and Developmental Biology, Journal Year: 2025, Volume and Issue: 13

Published: April 25, 2025

Glaucoma is a leading cause of irreversible blindness worldwide. Elevated intraocular pressure caused by restricted outflow the aqueous humor leads to degeneration retinal ganglion cells (RGCs) and their axons. Emerging evidence suggests that pathological mechanisms relating protein folding mitochondrial dysfunction are significant factors in disease onset different types open-angle glaucoma. In this review, we discuss these defects three distinct glaucoma: primary glaucoma (POAG), normal tension (NTG), exfoliation (XFG). Genetic mutations linked previously mentioned glaucoma, including those myocilin (MYOC), optineurin (OPTN), lysyl oxidase 1 (LOXL1), disrupt homeostasis, endoplasmic reticulum stress, activation unfolded response impaired autophagic degradation. These contribute trabecular meshwork cell apoptosis. addition defects, also associated with progression damage death RGCs. Factors such as oxidative an altered fission-fusion balance, mitophagy dysregulation make RGCs vulnerable optic nerve degeneration. The crosstalk between underscores complexity pathogenesis offers potential targets for therapeutic intervention. Strategies aimed at restoring enhancing function, mitigating cellular stress responses hold promise neuroprotection

Language: Английский

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